Abstract: Neuroinflammation, mediated by the reactivity of the system of cytokines, accompanies the flow of amyloidosis in Alzheimer’s disease, alongside with disturbances in the work of central departments of the olfaction analyzer. Therefore, it is advisable to determine the reactivity of the cytokine system in the brain sections of elderly rats (neocortex, hippocampus, olfaction bulbs, hypothalamus, caudate nuclei) under the conditions of the bulbar effect of β-amyloid peptide aggregates. The content of tumor necrosis factor α, interleukin-6 and interleukin-10 in the brain sections of the rats having the age of 18 months (n = 24) that are being studied was determined 5 days after the intrabulbar injection of the suspension of β-amyloid peptide 40 (Amyloid β Protein Fragment 1-40, Sigma-Aldrich, USA) in the bidistilate or the solvent itself. It has been shown that the initial level of activity of the cytokine system (intact animals of the control group, n = 8) in the brain sections that are tangent to the olfaction analyzer (neocortex, hippocampus and olfactory bulbs) is probably lower in comparison to other parts (hypothalamus and caudate nucleus) of elderly rats. Intraubulbar injection of β-amyloid peptide 40 aggregates to elderly rats (experimental group, n = 8) increases the activity of the cytokine system in the brain structures distant from the spot of injection (neocortex and hippocampus) responsible for memory mechanisms. It has been determined that the reactivity of the cytokine system in the neocortex, hippocampus and hypothalamus is higher not only in response to the specific toxic effects of the β-amyloid peptide 40 aggregates (experimental group, n = 8), but also due to surgical intervention with the injection of solvent alone (comparison group, n = 8). It has been generalized that the low content of pro- and anti-inflammatory cytokines in phylogenetically younger parts of the brain (neocortex, hippocampus) of intact animals corresponded to increased reactivity of the cytokine system under the influence of exogenous β-amyloid peptide 40.